Abstract
Polychlorinated biphenyls (PCBs) are well-known recalcitrant environmental pollutants. Although the metabolism of the PCBs has been intensively studied, very little is known about their mechanism of toxicity in living organisms or how they are degraded. We have examined the effects of PCBs on two different yeast strains to determine their mechanism of action. One yeast strain (K 601, wild type) is resistant to the growth-inhibitory effect of PCBs, whereas the other strain (AA 542, PMR 1 mutant) is susceptible. PCBs increased the level of intracellular hydrogen peroxide in AA 542 cells but not in K 601 cells. In the presence of α-tocopherol or ursolic acid the growth of AA 542 cells was not inhibited by treatment with PCBs. These results suggest that PCBs block cell growth through production of hydrogen peroxide in the PMR 1 mutant strain, AA 542. We compared superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities in both strains. The catalase activity in K 601 cells was 10 times higher than that in AA 542 cells. In contrast, there was no difference in activities of SOD and GPx between the two strains. Collectively, these observations indicate that oxidative stress causes the inhibition of cell growth observed in catalase-deficient yeast cells exposed to PCBs.
